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Cardiovascular Research 2007 73(3):470-480; doi:10.1016/j.cardiores.2006.09.005
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Copyright © 2006, European Society of Cardiology

Phagocytosis in atherosclerosis: Molecular mechanisms and implications for plaque progression and stability

Dorien M. Schrijvers*, Guido R.Y. De Meyer, Arnold G. Herman and Wim Martinet

Division of Pharmacology, University of Antwerp, Universiteitsplein 1, B-2610 Wilrijk, Belgium

* Corresponding author. Tel.: +32 3 820 27 10; fax: +32 3 820 25 67. Email address: dorien.schrijvers{at}ua.ac.be

Macrophages play a key role in atherosclerotic plaque destabilization and rupture. In this light, selective removal of macrophages may be beneficial for plaque stability. However, macrophages are phagocytic cells and thus have an important additional role in scavenging of modified lipoproteins, unwanted or dead cells and cellular debris via phagocytosis. The concept of phagocytosis as well as the underlying mechanisms is well defined but the effect of phagocytosis in terms of plaque stability remains poorly understood. Recent findings point towards a complex role of macrophage phagocytosis in atherogenesis. Macrophages are necessary for removal of apoptotic cells from plaques, but exert strong proatherogenic properties upon phagocytosis of lipoproteins, erythrocytes and platelets. Apart from heterophagy, autophagocytosis better known as autophagy may occur in advanced atherosclerotic plaques. Several lines of evidence indicate that autophagy is initiated in plaque smooth muscle cells as a result of cellular distress. Since autophagy is well recognized as a survival mechanism, autophagic smooth muscle cells in the fibrous cap may reflect an important feature underlying plaque stability. All together, phagocytosis is a crucial process involved in atherogenesis that may significantly affect the stability of the atherosclerotic plaque.

KEYWORDS Atherosclerosis; Phagocytosis; Lipoproteins; Apoptosis; Plague stability

Time for primary review 17 days


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